Scientists in Cambridge, UK, using a mouse with a human chromosome in its cells, discovered that gene expression, contrary to what was previously thought, is mostly controlled by regulatory DNA sequences.
Mice and humans (and most vertebrates) share the majority of their genes but a distinct gene regulation – so, when and where these shared genes become activated – assures their many individual characteristics, and knowledge of this regulation is crucial if we want one day to be able to control gene expression.
A new improved gene therapy can be the first treatment for Machado-Joseph disease
Portuguese, Swiss and French researchers show, for the first time, that is possible to inhibit, in a living organism, the mutated copies of a gene without affecting any existing normal copies of the same gene. The research, to appear in the 8th of October edition of the journal PLoS One, describes how scientists successfully used the approach in rats to reverse the symptoms of Machado Joseph Disease (MJD), an untreatable and potentially fatal neurodegenerative disease.
Religious emotions and beliefs have often been linked to a capacity to deal with pain, as those
images of Philippine men being willingly crucified during religious festivals so well demonstrates. But although changes in pain sensitivity during a religious experience are well documented, the exact psychological or/and neurological reasons of the phenomenon are unclear and, as such, have now become the aim of an investigation by a group of scientists, philosophers and psychologists from the University of Oxford.
The research, to be published in the next edition of the journal Pain, reveals for the first time that religion-associated pain resistance is linked to the activation of the brain right ventrolateral prefrontal cortex (VLPFC), an area associated with both cognitive down-regulation of pain and reassessment of the emotional meaning of an experience – for example by giving a neutral or even positive meaning to a noxious experience, and so making it much easier to cope with.
For a long time scientists have been puzzled by the fact that the immune system in the gut is capable of fighting toxic bacterial infection while staying, at the same time, tolerant to its resident “friendly” bacteria. But an article now published in the journal Cell Host & Microbe(1) is starting to open the door to this mystery by revealing how a recently discovered gene - pims – is activated by the gut immune response against friendly bacteria to rapidly suppress it, effectively creating tolerance to the gut microbiota.
In the same way pims is also shown to control the magnitude of immune responses against toxic bacteria by suppressing immuno-reactivity when a certain activation threshold is achieved, assuring, in this way, that the response stays restricted to the infection site and is proportional to the extent of the infection. These results suggest that the balance tolerance/immuno-reaction in the gut is achieved through self-regulatory cycles where suppression by negative regulators, such as pims, is triggered as soon as a specific threshold of immuno activation is reached.
The architecture of haematopoiesis – which is the process by which all blood cells originate – is essentially the same throughout the mammal world, report scientists in the Proceedings of the Royal Society.
This is an unexpected result considering the thousands of mammals’ species with a myriad of habitats and lifestyles, as so well demonstrated when comparing the 30 mm flying bumblebee bat and the 30 metre-long aquatic blue whale both mammals.
But the work now published shows that the variations in the blood system - necessary to adapt to the evolutionary changes found within the mammals’ world -can be explained quantitatively (for example by producing more cells or having the cells dividing faster), and are directly correlated to the animals’ body mass and do not require any fundamental alteration in the haematopoietic process.
Why do humans cooperate in things as diverse as environment conservation or the creation of fairer societies, even when they don’t receive anything in exchange or, worst, they might even be penalized? This is a question that has puzzled academics for centuries, especially since in evolution the basis for the “survival of the fittest” is, after all, selfishness.
But in an article just published in the journal Nature, three Portuguese theoretical physicists developed a mathematical model capable of providing a way out from this conundrum through the introduction of social diversity - a ubiquitous characteristic of modern social networks - and suggesting that that the act of cooperation may depend on one’s social context/ranking. And in fact, when social diversity was taken into account the numbers of those cooperating increased in direct relation to the system diversity.